Autophagy at the crossroads of catabolism and anabolism

Autophagy at the crossroads of catabolism and anabolism

2015-08-01 | Kaur, Jasvinder; Debnath, Jayanta
The article "Autophagy at the Crossroads of Catabolism and Anabolism" by Jasvinder Kaur and Jayanta Deb Nath, published in *Nature Reviews Molecular Cell Biology*, discusses the multifaceted role of autophagy in cellular metabolism and homeostasis. Autophagy, a conserved catabolic process, degrades cytoplasmic components and organelles in lysosomes. While protein degradation is a key feature, recent studies highlight its role in mobilizing diverse cellular energy and nutrient stores, such as lipids, carbohydrates, and iron. The review covers the established and emerging roles of autophagy in fueling biosynthetic capacity and promoting metabolic and nutrient homeostasis. Key points include: - **Autophagosome Biogenesis**: The process of autophagosome formation involves initiation, nucleation, and expansion stages, regulated by various proteins and lipid modifications. - **Selective Autophagy**: This process targets specific cargoes like mitochondria, peroxisomes, and protein aggregates, mediated by autophagy cargo receptors. - **Protein Degradation and Synthesis**: Autophagy-derived amino acids are crucial for maintaining protein synthesis and energy production, particularly during stress conditions. - **Lipophagy**: The selective degradation of lipid droplets releases fatty acids for β-oxidation and the TCA cycle, contributing to energy production. - **Carbohydrate Metabolism**: Autophagic degradation of glycogen maintains glucose homeostasis, and disruptions in this process are linked to genetic myopathies. - **Ferritinophagy**: The degradation of ferritin mobilizes bioavailable iron, essential for various cellular processes. The article emphasizes the importance of autophagy in maintaining cellular function and viability, particularly in response to stress and nutrient deprivation. It also highlights the potential therapeutic implications of understanding and manipulating autophagy in diseases such as cancer and metabolic disorders.The article "Autophagy at the Crossroads of Catabolism and Anabolism" by Jasvinder Kaur and Jayanta Deb Nath, published in *Nature Reviews Molecular Cell Biology*, discusses the multifaceted role of autophagy in cellular metabolism and homeostasis. Autophagy, a conserved catabolic process, degrades cytoplasmic components and organelles in lysosomes. While protein degradation is a key feature, recent studies highlight its role in mobilizing diverse cellular energy and nutrient stores, such as lipids, carbohydrates, and iron. The review covers the established and emerging roles of autophagy in fueling biosynthetic capacity and promoting metabolic and nutrient homeostasis. Key points include: - **Autophagosome Biogenesis**: The process of autophagosome formation involves initiation, nucleation, and expansion stages, regulated by various proteins and lipid modifications. - **Selective Autophagy**: This process targets specific cargoes like mitochondria, peroxisomes, and protein aggregates, mediated by autophagy cargo receptors. - **Protein Degradation and Synthesis**: Autophagy-derived amino acids are crucial for maintaining protein synthesis and energy production, particularly during stress conditions. - **Lipophagy**: The selective degradation of lipid droplets releases fatty acids for β-oxidation and the TCA cycle, contributing to energy production. - **Carbohydrate Metabolism**: Autophagic degradation of glycogen maintains glucose homeostasis, and disruptions in this process are linked to genetic myopathies. - **Ferritinophagy**: The degradation of ferritin mobilizes bioavailable iron, essential for various cellular processes. The article emphasizes the importance of autophagy in maintaining cellular function and viability, particularly in response to stress and nutrient deprivation. It also highlights the potential therapeutic implications of understanding and manipulating autophagy in diseases such as cancer and metabolic disorders.
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